长期使用NSAID或他汀类对PSA无影响

圣迭戈——一项临床试验的二次分析结果表明，长期使用阿司匹林、其他非甾体抗炎药(NSAID)或他汀类药物，既不会影响前列腺特异性抗原(PSA)水平，也不会影响PSA水平变化速率。

“鉴于他汀类、阿司匹林和其他NSAID在一般人群中、尤其是在前列腺癌高危男性中的广泛使用，采用这些药物预防前列腺癌已成为一个热点话题。已有很多篇论文提示这些药物与癌症预防有关，但其结果并不一致，因此只有开展前瞻性研究才能最终确定这些药物对前列腺癌的影响。”

亚利桑那州癌症中心前列腺癌预防组组长、科学审查委员会主席Stratton医生及其同事对一项Ⅲ期化学预防试验中的699名男性受试者进行了分析。这项试验旨在了解硒补充剂对前列腺癌发病率的影响。

“硒不起作用，但我们在这项研究中还询问了男性受试者对其他常用药物(如他汀类和NSAID)的使用情况；我们在5年期间每6个月对所有男性检测一次PSA。我们采用统计学模型来判断这些药物的使用是否与PSA随时间的改变有关。”

这项研究中的男性受试者具有超过4 ng/ml的PSA水平和/或可疑的直肠指检结果和/或超过0.75 ng/ml•年的PSA变化速率(PSAV)，但前列腺活检结果为阴性。在研究过程中，73例受试者被诊断为前列腺癌。

在校正包括硒补充剂使用、年龄、种族、体重指数和年吸烟量等变量之后，研究者发现，阿司匹林、NSAID或他汀类药物的使用与PSA(分别P=0.79、0.68和0.79)或PSAV(分别P=0.23、0.43和0.84)均无明显关系。发生前列腺癌者和再次前列腺活检结果仍为阴性者的结果与总体结果一致。

“这项研究的随访时间不够长，也不是旨在检验这些药物的癌症预防效果，但鉴于可信区间相当窄，我们可以说这些药物的使用并不影响PSA检测。这非常重要，因为如果这些药物会干扰PSA检测——不论是否影响癌症本身——都会妨碍对服用这些药物的患者进行PSA检测。”

他承认这项研究存在某些局限性，包括这是利用针对其他问题的临床试验数据进行的二次分析，而且有关药物使用的数据是基于患者自我报告而不是基于其医疗记录或更严格的数据采集方法。

Stratton医生声称无相关利益冲突。

爱思唯尔版权所有  未经授权请勿转载

By: DOUG BRUNK, Internal Medicine News Digital Network

SAN DIEGO – Long-term use of aspirin, other nonsteroidal anti-inflammatory drugs, or statins affected neither the levels of prostate-specific antigen nor the velocity with which those levels changed, judging from a secondary analysis from a clinical trial.

"The prevention of prostate cancer by statins, aspirin, and other NSAIDs is an important topic given the widespread use of these drugs in the general population and particularly in the population of men at risk for prostate cancer," Steven P. Stratton. Ph.D., said in an interview during a conference sponsored by the American Association for Cancer Research and the Prostate Cancer Foundation.

"A lot of scientific papers have been published linking these drugs together with cancer prevention, but results are controversial. So definitive, prospective studies in prostate cancer have to be performed before we can know for sure," he said.

In an effort to investigate the effect of these medications on markers used to assess prostate cancer risk, Dr. Stratton and his associates analyzed a population of 699 men enrolled in a phase III chemoprevention trial that was designed to investigate the effects of selenium supplementation on prostate cancer incidence.

"The selenium didn’t work, but we also asked men in this study about their use of other commonly used drugs like statins and NSAIDs; and we measured the PSA on all of these men every 6 months for 5 years," said Dr. Stratton, who chairs the Scientific Review Committee and leads the Prostate Cancer Prevention Team at the University of Arizona Cancer Center, Tucson. "We used statistical models to see if there were relationships between drug use and PSA changes over time."

Men in the study had a PSA greater than 4 ng/mL and/or a suspicious digital rectal examination and/or a PSA velocity (PSAV) of greater than 0.75 ng/mL/year, but with a negative prostate biopsy. During the course of the trial, 73 of the study participants were diagnosed with prostate cancer.

After Dr. Stratton and his associates adjusted for variables including selenium use, age, race, body mass index, and pack-years of smoking, they found that the use of aspirin, NSAIDs, or statins did not demonstrate significant associations with PSA (P = .79, .68, and .79, respectively) or PSAV (P = .23, .43, and .84, respectively). Stratification between men who developed prostate cancer during the course of the study and those with repeated negative prostate biopsies did not alter the results.

"The study wasn’t long enough, nor was it designed to detect a cancer prevention effect of these drugs, but we can say with pretty good confidence that the drug use did not impact the PSA test – a problem called ‘detection bias’ – given that we saw no differences between men taking the drugs and those who did not," Dr. Stratton said. "This is important, because if the drug interfered with the PSA test – regardless of the impact on cancer – it could reduce the usefulness of the PSA test in men taking these drugs."

He acknowledged certain limitations of the study, including the fact that it was a secondary analysis using data from a clinical trial designed for another purpose. "Also, the data on medication use were based on self-reporting by the patients rather than an examination of their medical records or more stringent methods of data collection," he said.

Dr. Stratton said he had no relevant financial conflicts to disclose.